Idiopathic dilated cardiomyopathy is a severe condition that results in heart enlargement and impairment of the ventricular contractile function. It causes progressive congestive heart failure that in some patients eventually requires cardiac transplantation. The precise mechanisms leading to ventricular dilation and dysfunction are not well understood. Impaired energy metabolism in the failing human heart could be an important mechanism of functional deterioration. Free fatty acids are known to contribute 60% of the energy used in the normal heart. Congestive heart failure (CHF) is associated with increased systematic and cardiac norepeinephrine levels which has been demonstrated to impair glucose handling and to increase systemic levels of free fatty acids (FFA), An increase in plasma FFA levels has been demonstrated to affect substrate oxidation in normal men and diabetic patients. FFA released by catecholamine stimulation have been shown to augment myocardial oxygen consumption, a factor which may be relevant in the setting of limited oxygen delivery which are seen in heart failure. Despite the importance of myocardial metabolism, utilization of free fatty acids in patients with dilated cardiomyopathy remains unknown. The purpose of this study is to determine if myocardial fatty acids oxidation is increased in the cardiomyopathic compared to normal heart. Arteriovenous differences of stable isotopes of palmitate, glucose and lactate with calculation of uptake and oxidation, using coronary sinus blood flow measurements, will be compared at rest and with the increased myocardial oxygen demand of atrial pacing. Free fatty acids oxidation rates will be controlled for myocardial mass, cardiac output activity, dietary intake and body composition.